NUR 300: Urologic Problems I
Lecture Prep and Study Guide
Topic that will be covered in class today:
Required preparation before class
1. Glomerular disorders
1. Read Copstead: Ch. 27 (pp 673-
2. Chronic kidney disease and kidney failure 678); Ch. 28 (pp 690-694)
3. Pharmacotherapy in chronic kidney disease
Glomerular disorders
Define hematuria, azotemia, oliguria, and proteinuria
o Hematuria – Blood in the urine
o Azotemia – Increased BUN/symptoms associated
o Oliguria – Decreased urine output (less than ~400 mL/day)
o Proteinuria – Protein in urine
Define and discuss the important characteristics of glomerulonephritis, including where the
damage occurs.
o Defined: A variety of conditions that cause inflammation of glomeruli
o Characteristics
Affects both kidneys equally
3rd leading cause of kidney failure in the U.S.
Primarily an immune-mediated process
o Where damage occurs…
Glomerulus – Delicate network of arterioles within the Bowman’s capsule
Tubules – Massive consumer of oxygen
Alterations in glomerular capillary circulation
Discuss the layers of the glomerulus and how glomerulonephritis affects the basement membrane.
o Capillary membranes have 3 layers:
Endothelium
Basement membrane
Glomerulonephritis affects the basement membrane because immune cells
attack it
Podocytes (special epithelial cells)
Describe the 2 main etiologies of glomerulonephritis; what do these 2 etiologies have in common?
o Primary – related to kidney specifically
, Antibodies attach to antigens of the glomerular basement membrane (“anti-GBM
antibodies”)
Type 2 Hypersensitivity Reaction – reactions occur on the cell surface and result in
direct death or malfunction
o Secondary – related to other disease process
Antibodies react with circulating antigens and are deposited as immune Complexes
in the GBM
Type 3 Hypersensitivity Reaction – immune complexes are deposited into tissues and
the resulting immune destroys the tissue
o BOTH etiologies have this in common
Accumulation of antigens, antibodies, and complement
Complement activation results in tissue injury
Discuss the HARP clinical manifestations of glomerulonephritis.
o Hematuria
o Azotemia
o Retention (Sodium & water retention, oliguria, leads to HTN and edema)
o Proteinuria
Describe the triggers and pathogenesis of acute glomerulonephritis.
o Triggers
Infectious
Poststreptococcal infection
Nonstreptococcal infection (Bacterial, viral, parasitic)
Primary Disease
E.g. Berger disease
Complexes attacking kidney (not exactly attacking basement membranes
Multisystem Disease
E.g. Goodpasture syndrome, systemic lupus erythematosus (SLE), vasculitis
Considered more secondary
o Pathogenesis – Acute Glomerulonephritis
Trigger → immune complexes form → complement activated → release of mediators
→ tissue injury → Hematuria, Proteinuria, Decreased GFR
Differentiate acute from chronic glomerulonephritis. (Lewis, pp. 1073-1074)
o Glomerulonephritis
Clinical manifestations
Hematuria
Coffee/cola colored urine (r/t breakdown of blood through tubules)
Oliguria
Less than 400 mL/day
Fluid retention
Lecture Prep and Study Guide
Topic that will be covered in class today:
Required preparation before class
1. Glomerular disorders
1. Read Copstead: Ch. 27 (pp 673-
2. Chronic kidney disease and kidney failure 678); Ch. 28 (pp 690-694)
3. Pharmacotherapy in chronic kidney disease
Glomerular disorders
Define hematuria, azotemia, oliguria, and proteinuria
o Hematuria – Blood in the urine
o Azotemia – Increased BUN/symptoms associated
o Oliguria – Decreased urine output (less than ~400 mL/day)
o Proteinuria – Protein in urine
Define and discuss the important characteristics of glomerulonephritis, including where the
damage occurs.
o Defined: A variety of conditions that cause inflammation of glomeruli
o Characteristics
Affects both kidneys equally
3rd leading cause of kidney failure in the U.S.
Primarily an immune-mediated process
o Where damage occurs…
Glomerulus – Delicate network of arterioles within the Bowman’s capsule
Tubules – Massive consumer of oxygen
Alterations in glomerular capillary circulation
Discuss the layers of the glomerulus and how glomerulonephritis affects the basement membrane.
o Capillary membranes have 3 layers:
Endothelium
Basement membrane
Glomerulonephritis affects the basement membrane because immune cells
attack it
Podocytes (special epithelial cells)
Describe the 2 main etiologies of glomerulonephritis; what do these 2 etiologies have in common?
o Primary – related to kidney specifically
, Antibodies attach to antigens of the glomerular basement membrane (“anti-GBM
antibodies”)
Type 2 Hypersensitivity Reaction – reactions occur on the cell surface and result in
direct death or malfunction
o Secondary – related to other disease process
Antibodies react with circulating antigens and are deposited as immune Complexes
in the GBM
Type 3 Hypersensitivity Reaction – immune complexes are deposited into tissues and
the resulting immune destroys the tissue
o BOTH etiologies have this in common
Accumulation of antigens, antibodies, and complement
Complement activation results in tissue injury
Discuss the HARP clinical manifestations of glomerulonephritis.
o Hematuria
o Azotemia
o Retention (Sodium & water retention, oliguria, leads to HTN and edema)
o Proteinuria
Describe the triggers and pathogenesis of acute glomerulonephritis.
o Triggers
Infectious
Poststreptococcal infection
Nonstreptococcal infection (Bacterial, viral, parasitic)
Primary Disease
E.g. Berger disease
Complexes attacking kidney (not exactly attacking basement membranes
Multisystem Disease
E.g. Goodpasture syndrome, systemic lupus erythematosus (SLE), vasculitis
Considered more secondary
o Pathogenesis – Acute Glomerulonephritis
Trigger → immune complexes form → complement activated → release of mediators
→ tissue injury → Hematuria, Proteinuria, Decreased GFR
Differentiate acute from chronic glomerulonephritis. (Lewis, pp. 1073-1074)
o Glomerulonephritis
Clinical manifestations
Hematuria
Coffee/cola colored urine (r/t breakdown of blood through tubules)
Oliguria
Less than 400 mL/day
Fluid retention
